A mitochondrial bioenergetic basis of depression

Klinedinst, N. Jennifer; Regenold, William T.

doi:10.1007/s10863-014-9584-6

Cited by 126 publications

(97 citation statements)

References 134 publications

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“…Elevated levels of adipic acid, and BCAAs, are known to be abnormal in ketoacidotic states (Liebich, Pickert, Stierle, & Woll, 1980). Meanwhile, a mutation in the LARS2 gene, which is responsible for the expression of mitochondrial Leucyl t-RNA synthetase has been found to occur in postmortem brain tissue of BD and SCZ patients (Munakata, Iwamoto, Bundo, & Kato, 2005) and which is thought to explain elevated levels of Lac in the brain (Ernst et al, 2017;Klinedinst & Regenold, 2014;Manji et al, 2012;Soeiro-De-Souza et al, 2016). Inadequate dietary (protein) intake, suggested by the decrease in BCAA, may be a risk-factor or a consequence of MDD.…”

Section: Pathway Analysismentioning

confidence: 99%

Biomarkers for major depressive and bipolar disorders using metabolomics: A systematic review

MacDonald¹,

Krishnan²,

Cervenka³

et al. 2018

American J of Med Genetics Pt B

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Major depressive disorder (MDD) and bipolar disorder (BD) lack robust biomarkers useful for screening purposes in a clinical setting. A systematic review of the literature was conducted on metabolomic studies of patients with MDD or BD through the use of analytical platforms such as in vivo brain imaging, mass spectrometry, and nuclear magnetic resonance. Our search identified a total of 7,590 articles, of which 266 articles remained for full-text revision. Overall, 249 metabolites were found to be dysregulated with 122 of these metabolites being reported in two or more of the studies included. A list of biomarkers for MDD and BD established from metabolites found to be abnormal, along with the number of studies supporting each metabolite and a comparison of which biological fluids they were reported in, is provided. Metabolic pathways that may be important in the pathophysiology of MDD and BD were identified and predominantly center on glutamatergic metabolism, energy metabolism, and neurotransmission.Using online drug registries, we also illustrate how metabolomics can facilitate the discovery of novel candidate drug targets. K E Y W O R D Sbiochemical, biomarker panel, mood disorders, omics

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Section: Pathway Analysismentioning

confidence: 99%

Biomarkers for major depressive and bipolar disorders using metabolomics: A systematic review

MacDonald¹,

Krishnan²,

Cervenka³

et al. 2018

American J of Med Genetics Pt B

View full text Add to dashboard Cite

show abstract

“…In summary, neurodegenerative disorders are a heterogeneous group of diseases [Doshi-Velez et al, 2014;Moore and Barker, 2014;Watts et al, 2014;Klinedinst and Regenold, 2015] that to date have defied molecular-targeted therapies [Calvo et al, 2014]. a-Lipoic acid [Gora˛ca et al, 2011;Keith et al, 2012] and butyrate have poor pharmacokinetic properties (short half-lives and first-pass hepatic clearance), and the multigram doses needed to achieve therapeutic concentrations in vivo , even if tolerable, are not feasible to administer.…”

Section: Traumatic Brain Injurymentioning

confidence: 99%

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Irwin

Moos

Faller

et al. 2016

Drug Development Research

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Preclinical Research In this review, we discuss epigenetic-driven methods for treating neurodegenerative disorders associated with mitochondrial dysfunction, focusing on carnitinoid antioxidant-histone deacetylase inhibitors that show an ability to reinvigorate synaptic plasticity and protect against neuromotor decline in vivo. Aging remains a major risk factor in patients who progress to dementia, a clinical syndrome typified by decreased mental capacity, including impairments in memory, language skills, and executive function. Energy metabolism and mitochondrial dysfunction are viewed as determinants in the aging process that may afford therapeutic targets for a host of disease conditions, the brain being primary in such thinking. Mitochondrial dysfunction is a core feature in the pathophysiology of both Alzheimer and Parkinson diseases and rare mitochondrial diseases. The potential of new therapies in this area extends to glaucoma and other ophthalmic disorders, migraine, Creutzfeldt-Jakob disease, post-traumatic stress disorder, systemic exertion intolerance disease, and chemotherapy-induced cognitive impairment. An emerging and hopefully more promising approach to addressing these hard-to-treat diseases leverages their sensitivity to activation of master regulators of antioxidant and cytoprotective genes, antioxidant response elements, and mitophagy. Drug Dev Res 77 : 109-123, 2016. © 2016 Wiley Periodicals, Inc.

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“…Depression affects an estimate of 350 million individuals worldwide (1) and is a serious public health problem due to its high morbidity, recurrence and suicide rate (2). Decades of extensive study of the pathophysiology of depression have led to various hypotheses regarding its molecular basis.…”

Section: Introductionmentioning

confidence: 99%

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

Gao

Zhu

et al. 2017

Exp Ther Med

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Abstract. Atractylenolide I (AT-I), a major component of the rhizoma of Atractylodes macrocephala Koidz., exerts a wide range of activities. The purpose of the present study was to investigate the anti-depressant-like effect of AT-I in a mouse model of chronic unpredictable mild stress (CUMS), and to explore the possible molecular mechanism involved. It was revealed that AT-I significantly ameliorated CUMS-induced depressive-like behaviors, as evidenced by increased sucrose preference as well as shortened immobility time in the forced swimming and the tail suspension test. In addition, AT-I reduced CUMS-induced decreases in the concentrations of serotonin and norepinephrine in the hippocampus. Furthermore, AT-I inhibited the activation of the nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome as well as the concentration of the pro-inflammatory cytokine interleukin (IL)-1β in the hippocampi of mice subjected to CUMS. In conclusion, the results of the present study suggested that AT-I exerts anti-depressant-like effects in a CUMS-induced model of depression in mice, the molecular mechanism of which is associated with the inhibition of NLRP3 inflammasome activation to decrease IL-1β production.

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A mitochondrial bioenergetic basis of depression

Cited by 126 publications

References 134 publications

Biomarkers for major depressive and bipolar disorders using metabolomics: A systematic review

Biomarkers for major depressive and bipolar disorders using metabolomics: A systematic review

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

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